Exploring the potential of laccase for endosulfan and chlorophacinone degradation: insights from molecular docking and molecular dynamics simulations.

Pesticides are widely used in agriculture but at the same time, a majority of them are known to cause serious harm to health and the environment. In the recent past, laccases have been reported as key enzymes having the ability to degrade pollutants by converting them into less toxic forms. In this investigation, laccase from polyextremophilic bacterium C-125 was analyzed for its structural, physicochemical, and functional characterization using in approaches.

Pharmacological inhibition of DNMT1 restores macrophage autophagy and M2 polarization in Western diet-induced nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is associated with an increased ratio of classically activated M1 macrophages/Kupffer cells to alternatively activated M2 macrophages, which plays an imperative role in the development and progression of NAFLD. However, little is known about the precise mechanism behind macrophage polarization shift. Here, we provide evidence regarding the relationship between the polarization shift in Kupffer cells and autophagy resulting from lipid exposure.

Laccaic acid restores epigenetic alterations responsible for high fat diet induced insulin resistance in C57BL/6J mice.

Laccaic acid, the major constituent of the food colouring agent-lac dye, possesses antioxidant and anti-inflammatory properties. Here we have evaluated the effects of laccaic acid on the high-fat diet induced insulin resistance in C57BL/6J mice. Insulin resistance was developed in mice by feeding high-fat diet for 12 weeks.

A small molecule potent IRAK4 inhibitor abrogates lipopolysaccharide-induced macrophage inflammation in-vitro and in-vivo.

Increasing evidence supports vanillin and its analogs as potent toll-like receptor signaling inhibitors that strongly attenuate inflammation, though, the underlying molecular mechanism remains elusive. Here, we report that vanillin inhibits lipopolysaccharide (LPS)-induced toll-like receptor 4 activation in macrophages by targeting the myeloid differentiation primary-response gene 88 (MyD88)-dependent pathway through direct interaction and suppression of interleukin-1 receptor-associated kinase 4 (IRAK4) activity. Moreover, incubation of vanillin in cells expressing constitutively active forms of different toll-like receptor 4 signaling molecules revealed that vanillin could only able to block the ligand-independent constitutively activated IRAK4/1 or its upstream molecules-associated NF-κB activation and NF-κB transactivation along with the expression of various proinflammatory cytokines.

Binge alcohol consumption exacerbates high-fat diet-induced neurobehavioral anomalies: Possible underlying mechanisms.

The current study aimed to validate the mice model of alcohol (ALC), high-fat diet (HFD), and HFD + ALC combination affecting neurobehavioral and neurochemical anomalies via inflammatory cascade, lowered neurogenesis, enhanced microgliosis, reactive astrogliosis, activated IDO-1 (indoleamine 2,3-dioxygenase), and reduce CHAT (choline acetyltransferase) signaling in the hippocampus (HIP). The adult male Swiss albino mice were provided with ALC (3-15%) and in-house prepared HFD for continuous 12 weeks. The HFD and HFD + ALC consumption impacted the liver and mediated HIP damage.

Lipid-induced monokine cyclophilin-A promotes adipose tissue dysfunction implementing insulin resistance and type 2 diabetes in zebrafish and mice models of obesity.

Several studies have implicated obesity-induced macrophage-adipocyte cross-talk in adipose tissue dysfunction and insulin resistance. However, the molecular cues involved in the cross-talk of macrophage and adipocyte causing insulin resistance are currently unknown. Here, we found that a lipid-induced monokine cyclophilin-A (CyPA) significantly attenuates adipocyte functions and insulin sensitivity.

Selenium-Enriched Probiotic Alleviates Western Diet-Induced Non-alcoholic Fatty Liver Disease in Rats via Modulation of Autophagy Through AMPK/SIRT-1 Pathway.

Current study was aimed to investigate the ability of L.acidophilus SNZ 86 to biotransform inorganic selenium to a more active organic form, resulting in trace element enrichment. Selenium-enriched L.

Cognitive deficits induced by combined exposure of stress and alcohol mediated through oxidative stress-PARP pathway in the hippocampus.

Several studies reported that stress can enhance the consumption of alcohol in humans and animals. However, the combinatorial effect of stress and alcohol on cognitive function and neurochemical alterations is quite understudied. In the present study, we have elucidated the involvement of oxidative stress-PARP cascade in alcohol and restraint stress (RS)-exposed animals using a PARP inhibitor, 1,5-isoquinolinediol (3mg/kg for 14days).

Small Molecule Inhibiting Nuclear Factor-kB Ameliorates Oxidative Stress and Suppresses Renal Inflammation in Early Stage of Alloxan-Induced Diabetic Nephropathy in Rat.

Diabetic nephropathy is one of the major microvascular complications of diabetes mellitus which ultimately gives rise to cardiovascular diseases. Prolonged hyperglycaemia and chronic renal inflammation are the two key players in the development and progression of diabetic nephropathy. Nuclear factor kB (NF-kB)-mediated inflammatory cascade is a strong contributor to the renovascular inflammation in diabetic nephropathy.

Edaravone alleviates cisplatin-induced neurobehavioral deficits via modulation of oxidative stress and inflammatory mediators in the rat hippocampus.

Cisplatin is a chemotherapeutic agent used in the treatment of malignant tumors. A major clinical limitation of cisplatin is its potential toxic effects, including neurotoxicity. Edaravone, a potent free radical scavenger, has been reported to have the neuroprotective effect against neurological deficits.

Piperine Augments the Protective Effect of Curcumin Against Lipopolysaccharide-Induced Neurobehavioral and Neurochemical Deficits in Mice.

The aim of the present study was to investigate the protective effects of curcumin alone and in combination with piperine against lipopolysaccharide (LPS)-induced neurobehavioral and neurochemical deficits in the mice hippocampus. Mice were treated with curcumin (100, 200, and 400 mg/kg, p.o.